Cargando…

SUN-405 From Diabetes Insipidus to Primary Polydipsia: The Dynamic State of Water Balance in Neurosarcoidosis

Background: Central diabetes insipidus (DI) may be transient and resolve days after pituitary surgery.Here we present the case of a patient with neurosarcoidosis who experienced resolution of his DI over a year after confirmatory testing, and unexpectedly developed primary polydipsia. Clinical case:...

Descripción completa

Detalles Bibliográficos
Autores principales: Haridas, Arjun, Belalcazar, Ligia
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Endocrine Society 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6553387/
http://dx.doi.org/10.1210/js.2019-SUN-405
Descripción
Sumario:Background: Central diabetes insipidus (DI) may be transient and resolve days after pituitary surgery.Here we present the case of a patient with neurosarcoidosis who experienced resolution of his DI over a year after confirmatory testing, and unexpectedly developed primary polydipsia. Clinical case: A 32 year old male was diagnosed with panhypopituitarism and neurosarcoidosis 14 months prior to admission when he presented with hypotension and acute encephalopathy. After receiving steroid and thyroid replacement, he improved but he developed polyuria, and had persisting hypernatremia and dilute urine. Patient underwent a water deprivation test which confirmed DI (had 100% increase in Uosm and had Uosm of >300 mosm/kg after desmopressin). He was discharged on Desmopressin 0.05mg daily, levothyroxine, hydrocortisone, and treatment for his neurosarcoidosis. Patient was again found nonresponsive and hypotensive, leading to most recent hospital readmission. He had a 1 week history of progressive weakness and lethargy and had been unable to take his medications for a few days prior to admission.The patient had completed 48 weeks of immunosuppressive therapy for his neurosarocidosis with prednisone (completed taper) and azathioprine (maintenance therapy) prior to admission. Lab testing showed a plasma sodium of 132mmol/L and a Uosm of 263mosm/kg. Patient was prescribed high dose IV hydrocortisone and levothyroxine. Desmopressin was held. MRI brain revealed leptomeningeal enhancement consistent with known neurosarcoidosis and steroids were switched to high dose prednisone. A week later, when patient’s mentation began to improve, he complained of increased thirst and polyuria (4.5L/day). His plasma sodium remained between 131-134mmol/L and urine was found to be consistently dilute (s.g.1.006-1.008). Team initiated IV fluids with saline and patient was drinking over 2 L of water per day. Patient’s sodium (off Desmopressin) reached a nadir of 128mmol/L and urine output increased to 5 L per day. Patient’s IV fluids were stopped and he was placed on water restriction (1.5L/day). Patient was discharged 10 days after stopping desmopressin, with improved mentation, a reduction in urine output (1.8 L/day); his plasma sodium ranged between 128 -130mmol/L and urine specific gravity of 1.008 confirming resolution of his DI and suggesting the development of primary polydipsia. Conclusion: Physicians should recognize the dynamic nature of water balance regulation in patients with panhypopituitarism due to neurosarcoidosis. Continuation of desmopressin without periodic evaluation of fluid and electrolyte balance may lead to the development of iatrogenic hyponatremia, particularly when DI resolves and dysregulation of patient’s thirst mechanism is present. Reference: Hypothalamo-pituitary sarcoidosis: a multicenter study of 24 patients QJM,Volume 105, Pages 981-995 C. Langrand et al.